Every year in the United States 10% of contact lens wearers experience contact lens associated red eye (CLARE), lowering the quality of life of millions of Americans. A related corneal affliction is microbial keratitis (MK), a potentially blinding disease that has left millions of people with vision loss worldwide. Host-pathogen interactions are a driving force in both afflictions. The ability of corneas to respond to disease s dependent upon our immune system and ability to heal wounds. Microbes (bacteria, fungi, and viruses) have employed numerous mechanisms for manipulating our immune system and basic physiology. Each of us is awash with microbes, yet our understanding of how these microbes communicate with our cells is poorly understood. The long-term goal of this research is to elucidate fundamental host-pathogen communication that is profoundly important for our well-being and instrumental for establishing disease. This study focuses on how a factor(s) secreted by Serratia marcescens inhibits corneal wound-healing by 1) identifying if these bacterial secreted factor(s) prevent wound healing in vivo in a rabbit corneal wound healing model and 2) testing the hypothesis the factor secreted by S. marcescens that inhibits corneal cell migration is lipolysaccharide. These answers may lead to therapeutic strategies for treating ocular infections and reduce infection-associated vision loss.